Evidence map›Paper›PMID 30038267›Full record

ArticleOncogene2018

USP17 mediates macrophage-promoted inflammation and stemness in lung cancer cells by regulating TRAF2/TRAF3 complex formation.

Chih-Hao Lu, Da-Wei Yeh, Chao-Yang Lai, Yi-Ling Liu, Li-Rung Huang, Alan Yueh-Luen Lee, S-L Catherine Jin, Tsung-Hsien Chuang

Erratum issuedAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Chih-Hao LuImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Da-Wei YehImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Chao-Yang LaiImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Yi-Ling LiuImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Li-Rung HuangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli, Taiwan.
Alan Yueh-Luen LeeNational Institute of Cancer Research, National Health Research Institutes, Miaoli, Taiwan.ORCID http://orcid.org/0000-0003-0252-0571
S-L Catherine JinDepartment of Life Sciences, National Central University, Zhongli District, Taoyuan City, Taiwan.
Tsung-Hsien ChuangImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan. thchuang@nhri.org.tw.ORCID http://orcid.org/0000-0002-5275-9022

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST 105-2314-B-400-006Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) MOST 105-2320-B-400-013-MY3National Health Research Institutes (NHRI) IM-106-PP-02National Health Research Institutes (NHRI) NHRI-EX106-10630SI
6 · The paper itself

Abstract

Macrophage accumulation and inflammation in the lung owing to stresses and diseases is a cause of lung cancer development. However, molecular mechanisms underlying the interaction between macrophages and cancer cells, which drive inflammation and stemness in cancers, are poorly understood. In this study, we investigated the expression of ubiquitin-specific peptidase 17 (USP17) in lung cancers, and role of elevated USP17 in the interaction between macrophages and lung cancer cells. USP17 expression in lung cancers was associated with poor prognosis, macrophage, and inflammatory marker expressions. Macrophages promoted USP17 expression in cancer cells. TNFR-associated factor (TRAF) 2-binding and TRAF3-binding motifs were identified in USP17, through which it interacted with and disrupted the TRAF2/TRAF3 complex. This stabilized its client proteins, enhanced inflammation and stemness in cancer cells, and promoted macrophage recruitment. In different animal studies, co-injection of macrophages with cancer cells promoted USP17 expression in tumors and tumor growth. Conversely, depletion of macrophages in host animals by clodronate liposomes reduced USP17 expression and tumor growth. In addition, overexpression of USP17 in cancer cells promoted tumor growth and inflammation-associated and stemness-associated gene expressions in tumors. These results suggested that USP17 drives a positive-feedback interaction between macrophages and cancer cells to enhance inflammation and stemness in cancer cells, and promotes lung cancer growth.

Indexed as

AnimalsCell Line, TumorHumansInflammationLung NeoplasmsMacrophagesMiceMice, Inbred C57BLNeoplastic Stem CellsTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3Ubiquitin-Specific ProteasesTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3Ubiquitin-Specific Proteases

Identifiers

PMID30038267
PMCPMC6283856

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.